Colony collapse disorder has been decimating bees for several years, but explanations have been hard to come by. After some spurious claims about cell phones causing the problem, researchers began identifying factors that did create problems for the health of bees, including infections, insecticides, and agricultural practices. The problem is that all of these seemed connected to colony collapse, which suggested the cause was likely to be complex.

Now, some researchers may have cut through the complexity. They've found that a common insecticide causes changes in the immune system of insects, which in turn leaves them more vulnerable to infection. And they've begun the process of determining how those immune changes come about on the molecular level.

The Italian researchers behind this current work previously analyzed an infection present in bees. But the concerns being raised about insecticides motivated them to look into whether there might be a connection between the two. Rather than focusing on bee mortality, they decided to look at the pathways that mediate immune responses in insects.

Bees lack that adaptive immune system that generates pathogen-specific antibodies and T cells in mammals. But they share an innate immune system, which is able to generally recognize infectious agents like bacteria. In fact, this innate immune system is evolutionarily ancient, as the same genes are used to control the response in animals as distantly related as bees and humans.

Previous toxicology work in mammals indicated that a specific class of insecticides, the neonicotinoids, could influence the activity of genes involved in the innate immune system. These genes were activated by the presence of neonicotinoids, and they shut down a key regulator of the innate immune system (a protein called NF-κb). Thus, the more of these insecticides, the less effective the innate immune system is likely to be—at least in mammals.

The researchers started by showing that the same is true in insects. Initially, they worked with everyone's favorite fruit fly, Drosophila, showing that the equivalent genes responded in the same ways in the flies. They then showed that the innate immune response isn't activated when these same flies are exposed to an infection. A different class of insecticide (an organophosphate) had a much weaker effect on the fly's innate immunity. With the molecular activity well characterized, they went on to demonstrate that the same effects could be seen in bees.

To show that the changes in gene activity had an impact on the bees' immune function, the authors turned to the deformed wing virus. Animals that were not given a dose of a neonicotinoid were able to largely keep the viral infection in check. But two different neonicotinoid insecticides showed a dose response: the more you gave the bees, the more likely the infection was to flourish.

If this result holds up, it neatly ties together a number of observations. Various infections may still be doing the ultimate job of killing the bees, but their virulence could be explained by compromised immune function, caused by a combination of insecticide use and agricultural practices. The results will also provide further support for the European Union's attempt to ban the use of neonicotinoid pesticides, a decision that was made earlier this year. Several chemical companies have announced that they will sue to block the ban.

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